The limitations in the present study include: (1) only male mice were used; (2) no studies were performed to determine the specific molecules in CagA-containing exosomes that could be primarily responsible for increasing ROS production and endothelial dysfunction and related mechanism(s); and (3) no studies were conducted to define the key pathway(s) that may significantly contribute to increased ROS levels in endothelial cells with CagA+H. This evidence concerns the gene S100A8 and endothelial dysfunction.